ArticleNature communications2021
Temporal evolution of cellular heterogeneity during the progression to advanced AR-negative prostate cancer.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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Who cites it
61 citing papers in PubMed, 87 citations in OpenAlex.
- Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1-mediated cell-intrinsic resistance.Nature communications · 2026Article
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- Crosstalk between EZH2 and DNA methylation mediates neuroendocrine prostate cancer lineage plasticity.Nature communications · 2026Article
- Genetic and epigenetic mechanisms underlying treatment-induced neuroendocrine prostate cancer.Journal of the National Cancer Center · 2026Review
- Transcriptional and epigenetic reprogramming, lineage plasticity and therapy resistance in prostate cancer.Journal of the National Cancer Center · 2026Review
- KDM4A promotes NEPC progression through regulation of MYC expression.Cancer letters · 2026Article
- Cellular plasticity and tumor ecosystem dynamics in prostate cancer: insights from single-cell and spatial transcriptomics.American journal of clinical and experimental urology · 2026Review
- The Quartet of Core Oncogenic Drivers in Neuroendocrine Prostate Cancer: Multi-Omics Dataset Integration to Forge a Translational Link Between Biology and Precision Therapy.International journal of biological sciences · 2026Review
- Mechanistic insights and molecular therapy for neuroendocrine prostate cancer.Frontiers in oncology · 2026Review
- Structural basis of DNA-dependent coactivator recruitment by the tuft cell master regulator POU2F3.Cell reports · 2025Article
- Seizure-Related Homolog Protein 6 (SEZ6): Biology and Therapeutic Target in Neuroendocrine Carcinomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- Lineage plasticity and histological transformation: tumor histology as a spectrum.Cell research · 2025Review
- Article
- Single-cell transcriptomics redefines focal neuroendocrine differentiation as a distinct prostate cancer pathology.Molecular oncology · 2025Article
- Lipid Nanoparticle Delivery of mRNA and siRNA for Concurrent Restoration of Tumor Suppressor and Inhibition of Tumorigenic Driver in Prostate Cancer.ACS nanoscience Au · 2025Article
- PROX1 is an early driver of lineage plasticity in prostate cancer.The Journal of clinical investigation · 2025Article
- Genetic variation modulates susceptibility to aberrant DNA hypomethylation and imprint deregulation in naive pluripotent stem cells.Stem cell reports · 2025Article
- The role of transcription factors in prostate cancer progression.Molecules and cells · 2025Review
- Defined cellular reprogramming of androgen receptor-active prostate cancer to neuroendocrine prostate cancer.bioRxiv : the preprint server for biology · 2025Article
- Deciphering Complexity: The Molecular Landscape of Castration-Resistant Prostate Cancer.Surgical pathology clinics · 2025Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Despite advances in the development of highly effective androgen receptor (AR)-directed therapies for the treatment of men with advanced prostate cancer, acquired resistance to such therapies frequently ensues. A significant subset of patients with resistant disease develop AR-negative tumors that lose their luminal identity and display neuroendocrine features (neuroendocrine prostate cancer (NEPC)). The cellular heterogeneity and the molecular evolution during the progression from AR-positive adenocarcinoma to AR-negative NEPC has yet to be characterized. Utilizing a new genetically engineered mouse model, we have characterized the synergy between Rb1 loss and MYCN (encodes N-Myc) overexpression which results in the formation of AR-negative, poorly differentiated tumors with high metastatic potential. Single-cell-based approaches revealed striking temporal changes to the transcriptome and chromatin accessibility which have identified the emergence of distinct cell populations, marked by differential expression of Ascl1 and Pou2f3, during the transition to NEPC. Moreover, global DNA methylation and the N-Myc cistrome are redirected following Rb1 loss. Altogether, our data provide insight into the progression of prostate adenocarcinoma to NEPC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.